Cholinomimetic teratogens are known to cause in chicken embryos muscular hypoplasia and defects of cervical, and other, vertebrae. This is basis of proposal. An extensive survey is planned of the role which acetylcholine activity, neuromuscular transmission and interference with these steps play in early chick development. The following specific problems to be studied: (1) the role played in neurotransmission of certain amino acids, such as gamma-aminobutyric acids, guanidine, etc., when combined with specific teratogen; (2) the effect of a recessive gene for muscular dystrophy of fowl on response to cholinomimetic compounds; (3) the interference by chloroquine with normal development of vertebrae and muscles and the role played by succinic dehydrogenase; (4) the possible beneficial effect of pralidoxime and pancuronium in prevention of developmental interference by cholinomimetic teratogens; (5) analysis of a complex syndrome cause by organophosphate insecticides and physostigmine (eserine) as it relates to acetylcholinesterase; (6) the role played by inorganic ions, such as calcium and potassium, in teratogenic steps other than those caused by cholinomimetic compounds, e.g. by carbonic anhydrase inhibitors; (7) the teratogenic nature of compounds mimicing acetylcholine, e.g. piperidine; (8) a study of certain antiserotonine componds, e.g. gramine, which cause teratogenic syndromes similar to those produced by cholinomimetic compounds; (9) to determine if componds that antagonize depolarization, such as benzoylcholine, will prevent the teratogenic activity of depolarizing teratogens, such as carbacol.